SIGNAL TRANSDUCTION MECHANISM OF INTERLEUKIN-6 IN CULTURED RAT MESANGIAL CELLS

被引：13

作者：

FUKUNAGA, M

FUJIWARA, Y

FUJIBAYASHI, M

OCHI, S

YOKOYAMA, K

ANDO, A

HIRANO, T

UEDA, N

KAMADA, T

机构：

[1] OSAKA UNIV,SCH MED,DEPT MED 1,1-1-50 FUKUSHIMA,FUKUSHIMA KU,OSAKA 553,JAPAN

[2] OSAKA UNIV,DIV 2,OSAKA,JAPAN

[3] OSAKA UNIV,SCH MED,BIOMED RES CTR,DIV ONCOL,OSAKA 553,JAPAN

来源：

FEBS LETTERS | 1991年 / 285卷 / 02期

关键词：

INTERLEUKIN-6; MESANGIAL CELL; SIGNAL TRANSDUCTION MECHANISM; PHOSPHOINOSITIDE TURNOVER; INTRACELLULAR CALCIUM; PROSTAGLANDIN-E2;

D O I：

10.1016/0014-5793(91)80813-I

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Interleukin 6 (IL-6) is one of the potent autocrine growth factors for mesangial cells. We investigated the signal transduction mechanism of IL-6 in cultured rat mesangial cells. IL-6 induced a transient increase of inositol 1,4,5-trisphosphate (Ins 1,4,5-P3) followed by a transient and sustained increase of intracellular calcium concentration, suggesting that IL-6 stimulates phosphoinositide turnover. IL-6 also stimulated prostaglandin E2 (PGE2) production. The IL-6-concentration dependency in PGE2 production was similar to that in Ins 1,4,5-P3 production. We concluded that the action of IL-6 on mesangial cells is exerted at least partially through the enhancement of phosphoinositide turnover and PGE2 production.

引用

页码：265 / 267

页数：3

共 12 条

[1] INOSITOL TRISPHOSPHATE, A NOVEL 2ND MESSENGER IN CELLULAR SIGNAL TRANSDUCTION [J].